Oxygen consumption and coronary reactivity in postischemic myocardium.

Abstract

Coronary vascular responses in regions of reversible postischemic myocardial contractile dysfunction (stunned myocardium) were examined in chronically instrumented, awake dogs. Left anterior descending coronary artery blood flow and oxygen extraction, aortic and left ventricular pressures, and regional myocardial segment shortening were determined. Regional myocardial blood flow was measured with microspheres. Coronary reactive hyperemia and vasodilator reserve, and regional myocardial oxygen consumption were determined. Three sequential 10-minute left anterior descending coronary artery occlusions separated by 30-minute reperfusion periods resulted in progressive postischemic dysfunction so that 1 hour after the final coronary artery occlusion, myocardial segment shortening was reduced to 37% of baseline. Despite this decrease in contractile function, left anterior descending artery flow (19.6 +/- 2.6 vs. 18.4 +/- 3.0 ml/min), myocardial blood flow and the transmural distribution of flow measured with microspheres, and regional myocardial oxygen consumption were unchanged. Although the coronary vasodilator reserve in response to adenosine was unaltered (63 +/- 9 vs. 70 +/- 15 ml/min), the reactive hyperemia response to a 10-second coronary occlusion was decreased in intensity (debt repayment ratio = 474 +/- 78% vs. 322 +/- 74%; p less than 0.05) and duration (57 +/- 9.1 vs. 35 +/- 4.5 seconds; p less than 0.05), while the peak flow response was unchanged (57 +/- 6.8 vs. 60 +/- 7.1 ml/min). Thus, in the intact awake animal postischemic myocardial contractile dysfunction was not associated with decreased myocardial oxygen consumption and did not impair the normal relation between coronary blood flow and myocardial oxygen utilization. Although coronary vessels showed a normal ability to vasodilate in response to adenosine, coronary reactive hyperemia was reduced.

Recovery of regional contractile function and oxidative metabolism in stunned myocardium induced by 1-hour circumflex coronary artery stenosis in chronically instrumented dogs.

“…The outcome of the reperfused myocardium will depend on the severity of the ischemic insult as well as on its duration. Brief episodes of intense myocardial ischemia of less than 25 minutes, induced by total coronary occlusion in the dog and k-ACETATE 16,19,22,23 From the above discussion, it is obvious that a definite diagnosis of stunning implies 1) documentation of complete recovery of contractile function after full reperfusion and 2) proof of absence of histological evidence for myocardial necrosis. Thus, in the strict sense, this diagnosis can only be made in retrospect.…”

Acute in vivo administration of a fish oil-containing emulsion improves post-ischemic cardiac function in n-3-depleted rats

“…However, a marked uncoupling between myocardial oxygen consumption and cardiac work was observed, mainly in the MCT:OO and saline groups. Several mechanisms can contribute to this mismatch, including mitochondrial dysfunction (30), heterogeneous microcirculation (31), desynchronized contractions (32), altered excitationcontraction coupling (33) and/or increased energy demand for contractile work (31). A shift toward increased utilization of fatty acids could also be considered (25).…”

Oxygen reperfusion is limited in the postischemic hypertrophic myocardium

“…Reversible or irreversible circulatory disturbances are frequently observed in the postischemic myocardium (9,27,29). Indeed, coronary flow decreased after ischemia in both SHR and WKY hearts.…”